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1. Adversive movements were induced by electrical stimulation and metrazol injection on area 4c of the cerebral cortex. 2. The adversive movement from area 4c does not pass through the thalamus, nucleus caudatus, nucleus lenticularis or superior collicuIus, but through direct efferent pathways in the internal capsule. 3. The adversive movement from area 4c passes through the pyramidal tract.

1) Cerebellar convulsion was identical with the cerebral cortical epileptic convulsion and the number of cases in which the march of spasm was observed were quite the same as that of cases in which convulsion occurred at the same time on the whole body. 2) No convulsion occurred by stimulation of the vermis cerebellaris and also convulsions occurred very rarely by that of the cerebellar nuclei. 3) In cases having the march of spasm caused by stimulation of the lobus lunatus anterior, spasm began in the fore limb, while by stimulation of the lobus lunatus inferior and lobus semilunaris spasm started mainly in the hind limb on the side of stimulation. 4) In the case of stimulation of cerebellum, the pathway of the impulse to the opposite side was considered to be the communication between both cerebellar hemispheres and both thalami and thus the march of spasm spread from one side of the body to the other side. 5) No march of cerebellar epileptic convulsion occurred without the cerebral motor cortex. 6) After the removal of both sides of the cerebral motor cortex no march occurred, but the general convulsion occurred. 7) No convulsion occurred by stimulation of the cerebellar hemisphere after the removal of both thalami or both nuclei lenticulares. 8) The march of convulsion occurs by close cooperation of the pyramidal and extrapyramidal tracts. It seems that for the impulse of the convulsion the extrapyramidal tract plays an important role, while for the start of the convulsion, that is, march of spasm pyramidal tract plays the main role.

March of spasm in epileptic convulsions was first observed by Tackson in 1863, when he said that in certain epileptic convulsions there is a phenomenon, where the convulsion starts from a certain muscle group and gradually spreads to other muscle groups. He called this, "march of spasm" and reported that it spreads according to the arrangement of motor representations in Rolando's area of the cerebral cortex. Since then, many important studies concerning the cerebral motor cortex were performed and reported. Recently, when Erickson had brought out a method in measuring electroencephalographic waves, Jackson's theory has been acknowledged. In Japan, Hayashi and his school has made an extensive study on epileptic convulsion. They used nicotine, cardiazol and others as chemical stimulations and decided the conduction tract of epileptic convulsion in dogs. The characteristic part of chemical stimulation is that, the nelve cells excite themselves when it is injected directly among them in certain concentrations and do not excite themselves when performed among nerve fibers. This was proved by Ishizuka. We used this method in dogs to see what was the mechanism of this phenomenon, "march" which is seen in epileptic convulsions and what tracts they took for conduction. And as its result, we found new facts that the presence of the motor cortex was needed for the march of spasm, and the conduction tract descending from the lenticular nucleus were quite different from Hayashi and his school had previously reported.

Anodal direct currents at intensities ranging from 0.3 to 30.0 microA were unilaterally applied for 30 min once a day to the premotor area of the rabbit cerebral cortex. The anodal polarization was repeated 10 times at intervals of 2-3 days, and the effect on the motor activity of the forelimbs during and after each polarization trial was compared with that before polarization. Peripheral motor activity was classified as either gentle flexion of forelimbs or struggle with violent movement of forelimbs. A current of 0.3 microA caused no change in motor behavior. Flexion of the forelimb contralateral to the polarized cortex was clearly increased when a polarizing current of 1.0 or 3.0 microA was applied, and peak flexion was observed between the third and seventh polarization trials. A current of 10 or 30 microA had no effect on forelimb flexion. Conversely, forelimb struggle on both sides was decreased when 10.0 or 30.0 microA, but not 1.0 or 3.0 microA, was applied. These results show that anodal polarization of the cerebral cortex exerts dual effects on peripheral motor activity, probably through changes in cortical excitability associated with the current intensity.